Diabetes Flashcards

Question

What is a Charcot foot? How is it investigated and managed?

Answer 1

Acutely: - A painful red swollen foot in a patient with diabetic neuropathy - Deformity e.g. 'rockerbottom feet' - Loss of function - Can be painful but surprisingly little/absent - especially given the extent of joint destruction Investigation: - Neurovascular assessment of the foot and ankle - HbA1C testing - Plain 2 view XR = evidence of bony deformity +/- osteomyelitis (e.g. periosteal reaction) - MRI (more sensitive for soft tissue or early stage osteomyelitis) Management: - Education re. joint damage and DM control - Immobilisation - with a cast, for 3-6/12 with repeated XR - Possible use of bisphosphonates - Surgery - for severe/unstable deformity that if untreated will result in amputation - Follow up podiatry with special orthotics for life Healing process takes c.1-2yrs - Prevent trauma, note temperature changes, check feet daily etc Manage any complications: - Fractures, neuropathic ulcers +/- infection/osteomyelitis; amputation

Answer 2

i) Thickening of basement membrane and increased permeability of retinal arteries → occlusion, aneurysm formation, increased exudates Blindness is common

Answer 3

Glomerular damage Ischemia of afferent/efferent arterioles Ascending infection i) Diabetic immunity often compromised – more susceptible to UTIs Renal hypertrophy Albuminurea – first detectable marker of diabetic nephropathy

Answer 4

Unsure aetiology (?) Types: i) Symmetrical mainly sensory = stocking and glove disruption ii) Acute painful = shins, worse at night iii) Mononeuropathy and mononeuritis multiplex = CN3+6 and carpal tunnel iv) Diabetic amyotrophy = progressive wasting of muscle tissue v) Autonomic neuropathy = CV and bladder problems, ED

Answer 5

Related to the duration and degree of hyperglycaemia – good control = fewer complications Glycation = addition of a sugar to a lipid through non-enzymatic means, leads to the accumulation of AGE’s (advanced glycation end-product) which are implicated in cell damage and inflammation i) Excess sugar means more AGE’s and greater negative effects Cells of retina, kidney and nerves do not require insulin for glucose uptake i) Excess glucose enters cells (excess glycation etc) Polyol pathway = excess glucose not put into the TCA cycle will be converted into sorbitol → fructose i) These cannot exit cells so draw water and other ions in down electrochemical gradients → affects cell functioning ii) Also produces ROS → direct cell damage Microvascular damage i) Narrowing of vessels → reduction in nutrients and oxygen ii) Accelerated by release of excess growth factors (VEGF) → more damage through over proliferation

Answer 6

First line = Diet + Exercise - can reverse a pre-diabetic state in this way Potential for: i) Metformin ii) Sulfonylurea iii) ‘Glitazones’ iv) Insulin

Answer 7

A state of impaired glycaemic control Categorised by: Fasting glu = <7.0mmol/l Post OGT 7.8-11.0mmol/l HbA1c = 5.7-6.4%

Answer 8

Metformin SE: N+V+D, stomach cramps, loss of appetite

Answer 9

Blood glucose - Self monitoring via finger prick test for those taking insulin - e.g. 4x per day (before each meal and once before bed, but depends on regimen and personal factors) - Increase monitoring during times of illness and watch for hyperglycaemia HbA1C – targets are variable: - e.g. 6.5%/48mmol for those on monotherapy with metformin, but increases slightly if on dual or triple therapy Blood ketones - Home blood monitor (NOT URINE, as less sensitive) BP: - At least once a year - Aim for 135/85 Weight: - Kept low/reduced - Reinforce dietary control Eyes: - At least once yearly checks for diabetic retinopathy Kidneys: - At least once yearly U+Es for albumin:creatinine and eGFR Feet: - At least once yearly podiatry review by specialist service Medication: - Understanding, adherence, side effects etc

Answer 10

Dieticians – carb counting Endocrinologists – long term management Diabetes specialist nurses – how to insulin, how to self-monitor, hypo/hyper management Podiatrists – foot care Ophthalmologists - eye care

Answer 11

``` If X has DM: Mother - 2% (though in mothers that develop DM before age 8 - same transmission risk as fathers) Father - 8% Both parents - 10% Sibling - 10% DZ twin - 15% MZ twin - 40% ``` Specific genetics - c.20 known associated e.g. HLADR3, HLADR4

Answer 12

If either mother or father has T2 then risk increases 15% If both have T2 then risk increases by 75% MZ twins - 10% DZ twins - 90% Thus more heritable than T1, though still not entirely genetically determined

Answer 13

1) Insulin deficiency + glucagon excess 2a) increased blood ketones - vomiting, acidosis, osmotic diuresis 2b) increased blood glucose - osmotic diuresis 3) fluid and electrolyte depletion - cellular dysfunction, shock, cerebral oedema

Answer 14

Check blood glucose to confirm symptom profile If conscious and patient able to swallow: 3-5 glucose tablets; 100-200mls fizzy drink/juice Wait 10 mins - if no response - repeat F/U with longer acting carb e.g. bread or biscuit Check BG in 15mins

Answer 15

As for mild if possible, if too unwell to cooperate: 0.5-1 tube of glucogel Wait 10 mins - if no improvement repeat F/U with longer acting carb, check BG in 15mins

Answer 16

At this point patient has a reduced level of consciousness +/- fitting: - do not attempt give anything PO With venous access: - 10% glucose with giving set, 50ml boluses Without IV access - Glucagon - SC or IM injections - If <5yrs = 0.5mg - If >5yrs = 1mg Wait 10mins When conscious - follow mild regimen

Answer 17

When people are frequently unable to notice when they are hypoing - puts them at risk of severe hypos + being in risky situations to hypo e.g. driving, crossing roads, cooking Common in people with T1 who have had it for a number of years; also common if have hypo’d recently within the last 2days; stress, depression and alcohol Also associated with certain medications e.g. beta blockers Managed with education and mindfulness; if frequent, may also be asked to increase window of glycaemic control - elevating target BG range (poss by changing how one uses insulin) prevent frequently dropping too low

Answer 18

Is postprandial hypoglycaemia - low blood sugar that occurs after a meal, usually within 4hrs of eating Cause for most is unknown - may depend on types of food or individual physiology/gut motility; also alcohol, surgeries e.g. for an ulcer, inherited metabolic disorders etc. Medical evaluation required to see if symptoms definitely reactive hypos; any known underlying cause corrected; ensuring you eat a balanced diet - all food groups, avoid sugary and processed carbohydrates e.g. white bread/pasta - esp on an empty stomach; eat food when you drink alcohol; snacking; insulin dose may need readjusting

Answer 19

Post hypoglycaemic hyperglycaemia Can be acute or chronic May be the result of high blood sugar in the morning due to excess insulin at night (too much insulin may make diabetes management unstable) Possible mechanism: prolonged hypo - physiological stress - glucagon + cortisol + adrenaline release - temporary insulin resistance - hyperglycaemia Rigorous BG monitoring including at night will help understanding - may need to readjust night doses

Answer 20

Different to - though often confused with - Somogyi rebound Early morning increase in blood glucose occurring between 8-10 hours of sleep secondary to cortisol/adrenaline/glucagon release and subsequent hyperglycaemia (so same mechanism but this one is sleep related whereas Somogyi doesn’t have to be sleep related)

Answer 21

Life expectancy reduced by 23 years DKA - 10x bigger killer than hypos 30-40% develop microalbuminaemia 25% require laser surgery for retinopathy Complications are worse for paediatric T2 25% of patients will have an amputation in their lifetime

Answer 22

Prevent hypo during exercise: - reduce insulin with meal before exercise = lower insulin conc. during and higher starting BG, less of a drop during (though hyper or delayed onset hypo may still occur later) - high intensity exercise burst - 10s intermittently throughout session or to top/tail= increase in adrenaline, raised glucose during and after exercise (may still late onset hypo) Post exercise - body is more sensitive to insulin (very sensitive within first 2hrs, waning over 48+hrs) - so increase potency of exogenous insulin and subsequent greater glu uptake Prevent hypo after exercise: - eat properly after - reduce insulin with meal after exercise = less insulin during ‘hot spot’ of insulin sensitivity, stable BG for c.8hrs (may be hyper or delayed hypo) - reduce basal insulin and insulin before and after exercise = less insulin to compensate for increased sensitivity, normal glucose during sleep without excessive carb intake and more stable glucose next day (working out reduction dose may require trial and error)

Answer 23

Need to have a BG of above 5 to drive - mornings can be hard sometimes - need to make sure you eat breakfast If hypo when driving - have to stop and wait 45 mins + BG of over 5 before they can drive again

Answer 24

t's worthwhile thinking of the average patient who is taking metformin for T2DM, you can titrate up metformin and encourage lifestyle changes to aim for a HbA1c of 48 mmol/mol (6.5%), but should only add a second drug if the HbA1c rises to 58 mmol/mol (7.5%) Dietary advice encourage high fibre, low glycaemic index sources of carbohydrates include low-fat dairy products and oily fish control the intake of foods containing saturated fats and trans fatty acids limited substitution of sucrose-containing foods for other carbohydrates is allowable, but care should be taken to avoid excess energy intake discourage the use of foods marketed specifically at people with diabetes initial target weight loss in an overweight person is 5-10% HbA1c targets This is an area which has changed in 2015 individual targets should be agreed with patients to encourage motivation HbA1c should be checked every 3-6 months until stable, then 6 monthly NICE encourage us to consider relaxing targets on 'a case-by-case basis, with particular consideration for people who are older or frail, for adults with type 2 diabetes' in 2015 the guidelines changed so HbA1c targets are now dependent on treatment: Lifestyle or single drug treatment Management of T2DM HbA1c target Lifestyle 48 mmol/mol (6.5%) Lifestyle + metformin 48 mmol/mol (6.5%) Includes any drug which may cause hypoglycaemia (e.g. lifestyle + sulfonylurea) 53 mmol/mol (7.0%) Practical examples a patient is newly diagnosed with HbA1c and wants to try lifestyle treatment first. You agree a target of 48 mmol/mol (6.5%) you review a patient 6 months after starting metformin. His HbA1c is 51 mmol/mol (6.8%). You increase his metformin from 500mg bd to 500mg tds and reinforce lifestyle factors Patient already on treatment Management of T2DM HbA1c target Already on one drug, but HbA1c has risen to 58 mmol/mol (7.5%) 53 mmol/mol (7.0%) Drug treatment The 2015 NICE guidelines introduced some changes into the management of type 2 diabetes. There are essentially two pathways, one for patients who can tolerate metformin, and one for those who can't: SEE DIAGRAMS Tolerates metformin: metformin is still first-line and should be offered if the HbA1c rises to 48 mmol/mol (6.5%)* on lifestyle interventions if the HbA1c has risen to 58 mmol/mol (7.5%) then a second drug should be added from the following list: sulfonylurea gliptin pioglitazone SGLT-2 inhibitor if despite this the HbA1c rises to, or remains above 58 mmol/mol (7.5%) then triple therapy with one of the following combinations should be offered: metformin + gliptin + sulfonylurea metformin + pioglitazone + sulfonylurea metformin + sulfonylurea + SGLT-2 inhibitor metformin + pioglitazone + SGLT-2 inhibitor OR insulin therapy should be considered Criteria for glucagon-like peptide1 (GLP1) mimetic (e.g. exenatide) if triple therapy is not effective, not tolerated or contraindicated then NICE advise that we consider combination therapy with metformin, a sulfonylurea and a glucagonlike peptide1 (GLP1) mimetic if: BMI >= 35 kg/m² and specific psychological or other medical problems associated with obesity or BMI < 35 kg/m² and for whom insulin therapy would have significant occupational implications or weight loss would benefit other significant obesity-related comorbidities only continue if there is a reduction of at least 11 mmol/mol [1.0%] in HbA1c and a weight loss of at least 3% of initial body weight in 6 months Practical examples you review an established type 2 diabetic on maximum dose metformin. Her HbA1c is 55 mmol/mol (7.2%). You do not add another drug as she has not reached the threshold of 58 mmol/mol (7.5%) a type 2 diabetic is found to have an HbA1c of 62 mmol/mol (7.8%) at annual review. They are currently on maximum dose metformin. You elect to add a sulfonylurea Cannot tolerate metformin or contraindicated if the HbA1c rises to 48 mmol/mol (6.5%) on lifestyle interventions, consider one of the following: sulfonylurea gliptin pioglitazone if the HbA1c has risen to 58 mmol/mol (7.5%) then a one of the following combinations should be used: gliptin + pioglitazone gliptin + sulfonylurea pioglitazone + sulfonylurea if despite this the HbA1c rises to, or remains above 58 mmol/mol (7.5%) then consider insulin therapy Starting insulin metformin should be continued. In terms of other drugs NICE advice: 'Review the continued need for other blood glucose-lowering therapies' NICE recommend starting with human NPH insulin (isophane, intermediate-acting) taken at bed-time or twice daily according to need Risk factor modification Hypertension blood pressure targets are the same as for patients without type 2 diabetes (see table below) ACE inhibitors or angiotensin II receptor blockers (ARB) are first-line an ARB is preferred if the patient has a black African or African–Caribbean family origin Clinic BP ABPM / HBPM Age < 80 years 140/90 mmHg 135/85 mmHg Age > 80 years 150/90 mmHg 145/85 mmHg Antiplatelets should not be offered unless a patient has existing cardiovascular disease Lipids following the 2014 NICE lipid modification guidelines only patients with a 10-year cardiovascular risk > 10% (using QRISK2) should be offered a statin. The first-line statin of choice is atorvastatin 20mg on

Answer 25

Drugs increase insulin release from islet cells so there is potential for hypos Hypos may last 24-48hrs due to drug half life 10% glucose infusions may be required continuously during this time - 100mls/hr - after the initial period of unconsciousness is treated If initial BG <1.3mmol/L - omit further doses until diabetes team R/V If initial BG 3-3.9mmol/L and not explained by a missed meal - reduce usual dose by 50%

Answer 26

Basal-bolus: - Quick acting insulin before meals + 1-2 medium/long acting insulins daily Twice daily: - Insulin mixtures BD; often with metformin in T2DM Once daily: - T2DM - Medium or long -acting insulin at bedtime together with oral hypoglycaemic agents

Answer 27

Metformin: (500mg OD with breakfast) - Decreases gluconeogenesis and increases peripheral utilisation of glucose; since it acts only in the presence of endogenous insulin it is effective only if there are some residual functioning pancreatic islet cells - SE: abdo discomfort, N+V; lactic acidosis, hepatitis; safe in pregnancy; avoid if eGFR <30; U+E annually Sulfonylureas: - e.g. gliclazide - Increase insulin secretion - SE: hypoglycaemia, GI discomfort; agranulocytosis; avoid in pregnancy Gliptins: - e.g. lina'gliptin' - (dipeptidylpeptidase-4-inhibitors) - Increase insulin secretion and lower glucagon secretion Pioglitazone: - (a thiazolidinedione) - Reduces peripheral insulin resistance - Several long term risks e.g. heart failure (CI) bladder Ca (CI) - SE: bone #, weight increase, visual impairment; avoid in pregnancy SGLT-2 inhibitors: - e.g. Canagli'flozin' - Reversibly inhibits Na-Glu transporter in PCT, reducing glucose reabsorption/increasing excretion - SE: UTI, DKA, hypoglycaemia, fornier's gangrene (genital/perianal nec fasc...) Glucagon-like peptide-1 receptor agonists: - e.g. Liraglu'tide' - Binds to this receptor - stimulating insulin secretion, suppressing glucagon secretion and slowing gastric emptying

Answer 28

1) Diet/lifestyle: - Low sugary foods, low fatty foods - Increase fibre intake, increase low fat dairy and oily fish - Aim to lose 5-10% of weight if overweight 2) Add metformin 3) Add one of: sulfonylurea OR pioglitazone OR gliptin OR SGLT-2 inhibitor 4) Add an additional one off the list 5) Metformin + sulfonylurea + GLP-1 mimic OR metformin + insulin regimen (e.g. NPH)